Se T OGI S| Mara CHAPTER 7 IMMUNE SYSTEM BIOO95 Centre of Foundation Studies 2021/2022 UiTM Cawangan Selangor, at Kampus DengkilLEARNING OBJECTIVES By the end of this chapter, students should be able to: 1.Classify the three lines of defence systemin human. 2.Describe the three external barriers. 3.Describe the four internal defences. 4.Describe the components of third line of defence. 5.Describe the events that occur during humoral immune response and cell mediated response. 6.Discuss immunodeficiencies in human. 7.Discuss the prevention of certain infectious diseases. un =Introduction B Immune system * Internal defense system- protects the body against foreign molecules by producing immune response. * pathogens —disease-causing organism( bacteria, fungus, virus and protozoa and worms) * must have the ability to distinguish self and non-self by unique proteins on surfaces of cells. * responds to signals from injured tissues, such as proteins released when cell membranes are damaged. 2un = 7.1: THREE LINES OF DEFENCETypes of defences Barrier defense: First lime prevent pathogens from gaining entrance to the body Internal defense: . Non-specific resistance Second line trrseoyeimecersina generalized way Adaptive immunity: Third line Zr" ="ve, Reguiros toveralOverview of animal immunity Barrier defenses: skin Mucous membranes Secretions Internal defenses: Phagocytic cells Natural killer cells Antimicrobial proteins Inflammatory response (Antibody-mediated immunity /Humoral response: ‘Antibodies defend against Infection in body fluids. Cell-mediated response: Cytotoxic cells defend against infection in body cells.immunity . . GeTCMer ste immunity ees ened leu ctnur Lol eMC LS} un -_— 7.1.1 EXTERNAL BARRIERS Rapid pt urgeBarrier defences Includes: 1. Skin, 2. Mucous membranes, 3. Secretions from the skin and mucous membranes. un =1. Skin * Is an impenetrable barrier. * Home to normal flora (non-pathogenic bacteria) that prevents the growth of pathogens un =1. Skin2. Mucous membranes + Are epithelial cells that line the digestive, respiratory, urinary and reproductive tracts. * Specialized cells that are scattered between the epithelial cells secrete mucus that trap pathogens. * The pathogens are eliminated by specific mechanisms. un =a) Mucous membranes that line the! ® digestive tract * Pathogens enter the stomach with food * The pathogens are destroyed by: * Stomach acids «Digestive enzymes in the intestine * Normal flora in the gastrointestinal tract un Sb) Mucous membranes that line the respiratory tract * The epithelial cells that line the respiratory tract also have cilia on its surface. * Pathogens present in inhaled air are trapped by the mucus within the trachea, bronchi and bronchioles. * The cilia sweeps the mucus upward towards the glottis to be swallowed into the digestive tract. un Sb) Mucous membranes that line the respiratory tract un -c) Mucous membranes that line the female reproductive tract * In female, the vagina = secretes sticky and acidic secretions that can kill pathogens. "promotes the growth of normal flora that prevents the growth of pathogens. un Sd) Mucous membranes that line the urinary tract * In both males and females, = Secretions from epithelial cells such as antibacterial agents inhibit bacterial growth. = Acidic urine also inhibits bacterial growth. = Urine cleanses the lower urinary tract/ urine flushes away pathogens in the tract. un S3. Secretions from the skin and mucous membranes. * Sweat, mucus, saliva and tears - hostile to many microbes. = oil and sweat glands give human skin a pH of 3-5, acidic to inhibit the growth of pathogens. = contain lysozyme that degrades bacterial cell walls. un S@ 7.1.2: INTERNAL DEFENCEBS Internal defence * Also known as the second line of defense * Is triggered when the pathogens enter the body * Four internal defences: Phagocytic cells Antimicrobial proteins Natural killer cells Inflammatory response Per un -1. Phagocytic cells * This type of defense is known as the cellular counterattack because the phagocytic cells (phagocytes) detect the pathogens and attack them. * Phagocytes kill the pathogens by engulfing them through phagocytosis. un =Phagocytosis 8 * Phagocytes have receptors that recognise certain structures such as polysaccharides on the bacterial cell wall. * Phagocytes engulf the bacteria and trap them in a vacuole. * The vacuole fuses with lysosome. + Lysosome produces nitric oxide (free radical) and other gases that poison the pathogens. + Lysozyme and other enzymes in the lysosome degrade the bacterial cell wall. UTM =Events of phagocytosis .@ Pseudopodia surround pathogens. © Pathogens are engulfed by endocytosis. '@ Vacuole forms. @ Vacuole and lysosome fuse. ‘© Pathogens destroyed. .@ Debris from pathogens released.OO - ( Macrophages » — a so oN —— ( Dendritic fe Phagocytic / ic \ cells ) \ cells D \ Neutrophils) Limited roles in es engulf and destroy phagocytosis ——__ pathogens Eosinophils) -Limited roles in orm phagocytosisMacrophages * Large, irregular shape of phagocytes known as ‘big-eaters, mye * Developed from monocytes in the blood NX * Patrol the body’s tissue ,engulfing damage cell and foreign matter. J + Others reside permanently in organs and tissues -example: lung’s air sac contain large no of macrophage to destroy foreign matter from air. meee un 2Dendritic cells * Roam in tissues that are in contact with the environment * Migrate to the lymph nodes after encountered pathogens * In the lymph nodes, dendritic cells interact with immune cells to stimulate adaptive immunity * Act as antigen presenting cells (APC) for T helper cells and activate cytotoxic T cells un =Neutrophils + The most abundant leukocytes * Circulate in the blood * Attracted to the injured sites by signals from infected tissues * Phagocytose bacteria before inactivated un =Eosinophils * Can be found in mucous membranes that line the digestive, respiratory and urinary tracts * Defend against multicellular invaders * Position themselves against the parasite’s body and destroy the parasites by secreting destructive enzymes un =2. Antimicrobial proteins Peptides and proteins that kill, prevent or inhibit the growth or reproduction of pathogens. * Includes: = Interferons = Complement system un =Interferons Proteins that inhibit viral reproduction. Secreted by virus-infected body cells. Stimulate uninfected cells to produce antiviral proteins that block viral reproduction. Help control viral infection such as cold and influenza by limiting cell- to-cell spread of viruses. Other type - interfering viruses, helping activate macrophages this enhances their phagocytosis. un =Virus (Go Vira uci acid Antiviral proteins block BS e 2 > viral reproduction New viruses Ointerferon genes turned on We DNA 7 ° Interferonstimulates a Interferon Df molecules » cell to turn on genes wy for antiviral proteins Host cell 1 Host cell 2 Makes interferon; Protected against virus is killed by virus by interferon fromcell 1 The interferon mechanism against viruses.Complement system * Isa group of approximately 30 proteins in blood plasma. * Circulate in an inactive form and are activated by substances on the surface of the pathogens. + The activation triggers the generation of membrane attack complex. + The complex insert themselves into the plasma membrane of the pathogens and form a lethal hole (pore). un =Membrane tine, rmirabe —complerent votes Activation of complement system and pore formation unComplement system * Extracellular fluid enters the pathogens through the pore causing the pathogens to swell and burst. * Other complement proteins coat the surface of the pathogens to enhance phagocytosis of the pathogens by the macrophages. un =3. Natural killer (NK) cells * Large, granular lymphocyte, originate from bone marrow. * Destroy virus infected body cells and tumor cells by both innate and antibody-mediated process. * Release perforin (protein) that form pores on the membrane of target cells. * Also release granzymes (protein) that enter the cells and activate proteins in the cells which induce apoptosis. un =—— | a ae ee, "one (hee omnes ‘rimertene ‘heh ee od Somme ‘ene Gmocemoee nets ‘Seger ate soon Set Sec The killingaction of natural killer (NK) cell un4. Inflammatory response * Nonspecific response to infection or tissue injury. * Minor injury or infection causes local inflammatory response but more severe injury or infection may leads to systemic inflammatory response (fever). un =Local inflammatory response * Characterized by redness, warm, swelling (edema) and pain. * Mast cells at infected or injured sites release histamine that have two functions: 1. Causes vasodilation of nearby blood vessels. 2. Increases the permeability of nearby capillaries. un =Local inflammatory response 1. Vasodilation of local blood vessels increases the blood flow to the injury site. * This causes the area to become: = Red because more blood flows to the site. = Warm because more metabolic heat is carried by the blood. un =Local inflammatory response 2. Increased capillary permeability leads to the release of fluid, blood clotting elements and phagocytes (monocytes and neutrophils) to the injury site. * This causes: = Edema (tissue swelling). = Pain because of the pressure on nerve endings on the region due to edema. un SLocal inflammatory response * Blood clotting elements will wall off inflamed area to prevent or delay the pathogens or toxic from spreading into surrounding tissues. * Neutrophils * carry out phagocytosis . =secrete signalling molecules that attract monocytes which will differentiate into macrophages to carry out phagocytosis. un SLocal inflammatory response * Activated neutrophils and macrophages release cytokines that increase blood flow to the injury site which also leads to redness and warmth. * Phagocytosis by the phagocytic cells leads to formation of pus that is a mixture of dead pathogens, tissue cells and phagocytic cells. un SMajor events in a local inflammatory response Neutrophil Qphistamines and cytokines @Antimicrobial released. Capillaries dilate, ~ peptides enter tissue. jeutrophils are recruited. un QNeutrophits ligest pathogens and cell debris. Tissue heals.Systemic inflammatory response 8 * Toxins released by pathogens and pyrogens produced by macrophages lead to an increase in body temperature (greater than 37.2°C/98.6°F) causing fever Inhibits the growth of Promotes some pathogens by Accelerates tissue phagocytosis by stimulating the liver and _ repair by speeding up phagocytic cells spleen to store iron so that | chemical reactions blood iron level is reduced ee un =7.1.3: THIRD LINE OF DEFENSE : COMPONENTS OF THIRD LINE OF DEFENSE un =Adaptive Immune Response (Acquired immuni FP Is a specific defence system which also known as a third line of defence. Detects a very specific pathogens using a small group of receptor proteins. Slower response. Is activated after innate immunity takes effect. Found in vertebrates. Two types : antibody-mediated immunity (humoral immune response) and cell- mediated immunity. un =UT Ey aN aL Le ie) eer) Cee ae Peer) Poem Oe ea) and clonal selection of B Pee feed EcrigMajor characteristics of adaptive immune response Ce nee ura) Peat Bet Eat) Pe ie) as ee eet raceeree rs Bee Be cells specific for Fries cii Dee ta Dea cl encountered i SCells Involved in Adaptive Immune Responses * There are two key cell types: lymphocytes and antigen-presenting cells (APC). * Lymphocytes include T lymphocytes (T cells), and B lymphocytes (B cells). * T cells and B cells recognize antigens. * All lymphocytes develop from stem cells in the bone marrow—B8 cells complete development in adult bone marrow; T cells mature in the thymus gland. * Roam in tissues and organs of the lymphatic system to induce immune response * Bind to antigen and undergo clonal selection to produce clone of cells un =uT— S Lymphocytes Bells Mature in the bone marrow Secrete antibodies T cells Mature in the thymus Directly attack the cells infected with pathogens Mount the antibody-mediated immunity Mount the cell-mediated immunity Two types: -T cytotoxic cells (T,) cells that destroy cells infected with pathogens -T helper cells (T,)cells that activate B cells and cytotoxic T cells by secreting cytokinesAntibody-mediated immunity Antigen receptor cell-mediated immunity as Thymus Antigen receptor Lymph nodes, spleen, and ‘ther lymphatic ‘organs un ~ Finalmaturation of BandT cells in lymphaticorgan unnanoieats The development of 8 colle and T cellsT-cell receptor (TCR) and B-cell receptor * A protein that is bounded to the membrane of the T cells and B cells, respectively. * TCR binds to antigen fragment that is displayed or presented on the surface of host cells by major histocompati 'y complex (MHC). * B cell receptor binds to antigenic determinant/epitope of intact antigen on pathogen or circulating free in body fluid. un ST cell receptor (TCR) and B cell receptor Poe iv rn 2 Beal (2 AB atc cof onan and no OVA Tet wont crt moan dere ste gh chanted ty rl oats Oe Behan ray cise tee unPathogen * An organism/virus that causes disease. Antigen * Substance that elicits immune response. * Has several different antigenic determinants (epitopes) on its surface - induce an immune response, recognised by different T cell and B cell receptors. * The binding of antigen to B cell receptors initiate the production of antibodies from the plasma cells. 2Antigen * Alarge molecule, either proteins or polysaccharides. * Recognised by lymphocytes. * — Elicits a specific immune response. * May be: * Components of pathogens such as toxins that are released in the extracellular fluid. = Proteins or glycoproteins on the surface of pathogens, foods or pollens such viramam a5 on the surface of transplanted organs.Antibody * Also known as immunoglobulin (Ig). + Isa protein secreted by B cells. * Has antigen-binding site that is complementary with the antigenic determinant/epitope found on antigen. * Binds to an intact antigen. + Interferes with pathogen activity. UT = =Antibody A molecule Be Antigen- binding sites Antigenic Determinants / epitopes| Antibody B oO molecule ‘The binding of antibodies to antigenic determinantsAntibody Bes Antigen binding V : Variable region € :Constant region Copyright® 2008 Pearson Education Inc. Publishing as Pearson Benjamin Cummings. unAntigen Presenting Cells * Macrophages, dendritic cells, and B cells function as APCs that display foreign antigens and their own surface proteins. * APC activate T helper cells * APCs are inactive until their receptors recognize a particular molecular structures on pathogens—when activated, the APC ingests the pathogen. * Lysosomal enzymes degrade most of the bacterial antigens—the APC displays eraneyoneeens fragments on its cell surface with a type of self-molecule (Class II MHC). * The activated APC such as macrophage releases signaling molecules along with the displayed antigen, and present displayed antigens to T helper cells. * Dendritic cells that become APCs leave the epithelial lining and, guided by chemokines, migrate to the lymph nodes, where they activate specific T cells capable of responding to the antigen UiTM SSelf Recognition : Major Histocompatibility Complex (MHC) * The ability of the vertebrate immune system to distinguish self from non- self depends on major histocompatibility complex (MHC). * MHCis a protein encoded by a group of genes. * Binds to antigen fragment and displays the fragments on the host cell surface (antigen presentation). un SSelf Recognition : Major Histocompatibility Complex (MHC) Class | MHC Class Il MHC Found on all nucleated cells Found on B cells, macrophages and dendritic cells that act as antigen presenting cells (APC) Recognised by T cytotoxic cells Recognised by T helper cells un SInfected cell Microbe Antigen @ Antigen presenting associates cel with MHC Antigen molecule fragment ‘Antigen fragment Class I MHC Class II MHC molecule e molecule Teell T cell —_ QTcell receptor ee recognizes combination (a) T cytotoxic cell (b) T helper cell ey The interaction of T cells with antigen-presenting cellsSelf Recognition : Major Histocompatibility | ax: Complex (MHC) * Acts as self marker to enable the immune system to distinguish self from non-self. * The concept of self from non-self = Mature B and T cells can differentiate self antigen from non-self antigen. = Self antigen is found on the host cells and does not trigger an immune response. = Non-self antigen is found on foreign cells that enter the body and triggers an immune response. 77.2: PROCESS OF ANTIBODY- MEDIATED IMMUNITY / HUMORAL IMMUNE RESPONSE AND CELL-MEDIATED IMMUNITY un SProliferation of lymphocytes * BandT cells are activated when they bind to antigen via antigen receptors. * Once activated, a B cell or T cell undergoes multiple cell divisions. * Activated B cells and T cells proliferate into two types of clones: effector cells and memory cells. * Clonal selection is a process by which an encounter with an antigen selects which lymphocytes will divide to produce a clone of cells specific for a particular epitopes. un =Proliferation of lymphocytes Effector cells Memory cells Short-lived | Long-lived Respond immediately to Rapidly activated upon the antigen during the first second exposure to the exposure same antigen Represent primary | immune response Represent secondary immune response un =Primary and secondary immune response Primary immune response Secondary immune response Peaks about 10-17 days after Peaks about 2-7 days after initial exposure to the antigen subsequent exposure the same antigen The response is slower The response is faster un S=> Antibody concentration Second exposure to antigen x, Secondary immune first exposure response to toantigenY antigen X = SS SS EES First exposure to antigen Primary immune Primary immune response to response to antigen X antigen Y (Sl 7 4 21 28 E | 42 49 56 Time (days) The two phases of the acquired immune responseThe role of T helper cell a= * Enhances antibody-mediated immunity and cell-mediated immunity. * APC engulfs a bacterium and degrades the antigen into antigen fragment. * APC displays the antigen-MHC complex on its surface. T helper cell binds to the complex via TCR. + The binding triggers the APC to secrete cytokines to stimulate the T helper cell to produce its own cytokines. * Aclone of activated T helper cells and memoryT helper cells are produced. + Activated T helper cells secrete other cytokines that activate B cells and T cytotoxic cells. UTThe role of T helper cell ene of agate apr Ts “ntbode by plas cel) Conyrign © 2014 Person Education, ne. Publishing 3s Parson Benamin Cummingsjody-mediated immunity (Humoral Immune Response) MHC complex “Antigen Bacterium Antigen SB ‘a. APC takes in bacterium, breaks it down, and presents foreign antigens on its surface in combination with MHC class Il antigens. 1b. B cell independently combines with foreign antigens on surface of bacterium, but B cell is typically not active until stimulated by activated T,, cells. 2. T;, cells are activated when their receptors combine with foreign antigen-MHC antigen ‘complexes on APC. Signaling takes place via cytokines secreted by both cells. 3. Activated Ty, cell recognizes antigen-MHC complex on B cell. T,, cell secretes cytokines that activate B cell that has interacted with foreign antigen. B cell then divides, and subsequent divisions produce clone of identical cells.Antibody-mediated immunity (Humoral imme Response) B cells differentiate and become plasma cells and memory B cells. 5. Plasma cells secretes antibodies via lymph and blood to the infected region. 6. The antibodies are specific to the antigen that activate the original B cell. 7. Memory B cells remain in the lymph tissue after the infection has been overcome. un SAntibody-mediated immunity (Humoral Immune Response) : Summary un = vad oes pathogenHow antibody destroy antigen? * Antibodies do not kill pathogens; instead, they mark pathogens for inactivation or destruction. * In neutralization, antibodies bind to viral surface proteins, preventing infection of a host cell. * Antibodies may also bind to toxins in body fluids and prevent them from entering body cells. unNeutralization Blocking of ability of virus to bindto a host cell Virus uT7* In opsonization, antibodies bind to antigens on bacteria, present a readily recognized structure for macrophage and neutrophils and therefore triggering phagocytosis. * Antigen-antibody complexes may bind to a complement protein, which triggers a cascade of complement protein activation. Ultimately, a membrane attack complex forms a pore in the membrane of the foreign cell, leading to its lysis. un =Opsonization Macrophage Promotion of phagocytosis of bacteria by macrophages and neutrophils UTActivation of complement system and pore formation Flow of water and ions. \ Zo Binding of antibodies Membrane attack complex activates the complement —_forms pores in the foreign system cell’s membrane. The cell swells and lyses. unCell-mediated immunity 5 * Infected cell displays antigen fragment on its surface via class | MHC. * An activated T cytotoxic cell recognises and binds to the antigen- MHC complex via TCR. * The activated T cytotoxic cell releases perforin that form pores on the infected cell membrane. * The activated T cytotoxic cell then secretes granzymes that enter the cell through the pores and induces apoptosis. _—2The killing action of T cytotoxic cells on an infected host cell Cytotoxic T cell Released cytotoxic T cell Dying target cellPlasma Memor or a aD clas > Defendagainst—intraceta atnegene _—_— Yate, extacelsar pathog and canceun = 7.3: HOMEOSTATIC IMBALANCES IN THE IMMUNE SYSTEMHomeostatic imbalances * Homeostatic imbalances is disruption in immune system function. * Occurs when the immune system responds to self-antigens causing serious and some fatal diseases. * Can be divided into: a) immunodeficiency diseases b) autoimmune diseases and c) allergies (Crraaas)Immunodeficiency diseases * Is a disorder in which the immune system is lacking the ability to protect against pathogens. * Leads to frequent and recurrent infections and susceptible to cancers. un SImmunodeficiency diseases Inborn immunodeficiency (congenital) Acquired immunodeficiency (develops later in life) UT vm, ‘+ Results from genetic or developmental defect in the production of immune system cells or specific proteins + Example: Severe combined immunodeficiency disease (SCID) Shortage or absence of B and T cells The person is susceptible to pneumonia and meningitis that can be fatal oCan be treated by bone marrow and stem cell transplantation + Due to exposure to certain chemicals or biological agents such as cancers, drugs to fight autoimmune diseases or drugs to prevent transplant rejection + Example: Human immunodeficiency syndrome (AIDS) ‘© Human immunodeficiency virus (HIV) attacks helper T cells The number of helper T cells will decrease leading to a decrease in the number of B and cytotoxic T cells ‘The person is susceptible to infections and cancersAutoimmune disease * Is a disorder in which the immune system fights the body’s own cells causing inflammation and organ damage. * 2/3 of the people with this disease are women. * Influenced by gender, genetics and environment. Affect nerves, muscles, endocrine system and digestive system. * Example: rheumatoid arthritis. un =Rheumatoid arthritis * Adisease in which the cartilage and joints are damaged and inflamed * Causes deformed joints accompanied with muscle pain, weakness, fatigue, loss of appetite and weight loss un 2Allergies + Allergies are hypersensitive responses to allergens (antigens). * Allergens consist of various foods and drugs, insect venom, molds, fungal spores, dust mites, cosmetics and pollen grains. * Occurs in nasal passages, bronchi and skin * Example: Hay fever un* Occurs rapidly in response to the binding of antibodies to a tiny amount of allergens. * Excessive amount of IgE is produced in response to exposure to antigens. * The IgE binds to mast cells. * Upon subsequent exposure to the same antigen, the antigen cross-links two neighbouring IgE and this triggers the mast cells to release histamine. * The release of histamine causes increased vasodilation and capillary permeability. Symptoms result : mucosal edema, redness, rashes, runny nose, sneezing. * Can be treated using — antihistamines, epinephrine UiTMun Diinitiat contact ‘with allergen Tigers fom Ho Hfm AAR, eon 0 ‘apie tno cope Pein gd bin iy Allergic reaction” Allergen Histamine ‘and other ‘chemicals Allergic reactionInitial and wt subsequent exposure go A attergen f Mast (second exposure) @nitial exposure eee” * exposure Vesicle / Histamine UM © Cross-linking triggers release of histamine.un 2 7.4: INFECTIOUS DISEASES* Infectious diseases - caused by pathogenic microorganisms, such as bacteria, viruses, parasites or fungi. * can be infected through: = direct contact with a person who is sick. * indirect contact, when you touch something that has germs on it. = Insect vector- eg: Anopheles mosquito. = contaminated food, water, soil, or plants * http://www.who.int/topics/infectious_diseases/en/ un 2DENGUE IN ASIA THE NUMBER STORY HOTSPOTS IN ASIA QvAe UsTSOvERES gy INCREASED BY 90/09 30X¢ DINGuE CASES Couey PANN: TRVE OUT OF TORE HOM ASA ‘EASE BURDEN USSTBILION I ASIA ANNUALLY i fe cone ro NDS Cost Law ‘pelhemcor man SANOFI a 1. Dengue © Viruses are transmitted through the bite of infected Aedes aegypti and Aedes albopictus female mosquitoes — daytime. ©. -should be suspected when a igh fever (40°C/104°F) is accompanied by 2 of the following symptoms: severe headache, pain behind the ‘eyes, muscle and joint pains, nausea, vomiting, swollen glands or rash.Prevention + Wear neutral-coloured clothing, long-sleeved, breathable garments. * Removing containers and disposing of unwanted rubbish around the yard that may collect water. Store containers upside down. Let pots drain directly onto the ground (avoid using saucers or drip trays under pot plants). * Use of personal household protection — window screens, mosquito nets, long- sleeved clothes, insecticide treated materials, coils and vaporizers, surface spray. + Fumigation. * Vaccine - people living in some dengue endemic countries. https dno famat.org/country/malaysia/risk/dengue2. Tuberculosis (TB) 8 Tuberculosis (TB) is caused by bacteria (Mycobacterium tuberculosis) that most often affect the lungs. Tuberculosis is curable and preventable. ‘Tabscteria become inter in weight due to water oes (te sie of bacteria after water loss wil be several microns) TBbsctens — a Dilton T8 vcr) ever mine In i Sneezing and eoushing vn PatientPrevention * Immunization - TB vaccine, BCG, is often given to babies and children. * Improving the ventilation in indoor spaces - fewer bacteria in the air. * Using germicidal ultraviolet lamps to kill airborne bacteria in buildings (where people at high risk of tuberculosis live). * Treating latent infection before it becomes active. * Infected people - cough etiquette and respiratory hygiene. un =3. Hepatitis * Hepatitis is an inflammation of the liver. * In chronic hepatitis, liver inflammation continues for at least six months. * This condition may be mild and result in relatively little damage, or may be more serious, causing resulting in destruction of many liver cells. Some severe cases lead to cirrhosis and eventually liver failure. un =uT—1 F Hepatitis is a risk for Dee R UT IL é O14 Caml Hepatitis B a Travel to endemic regions, can pu vavelers at risk 48 million http//magazine scientfiemalaysian.com/issue-9-2014/introduction-chronic-hepatts/How hepatitis spread? * Hepatitis A: - the transmission is fecal/oral. - Common in areas of poor sanitary conditions. - Epidemics can occur in situations of water contamination. * Hepatitis B: - Transmission occurs via body fluids (blood, semen, etc). - High risk groups include medical personnel, male homosexuals and dialysis patients. * Hepatitis C: - The virus is usually spread by direct contact with the blood of an infected person, including sharing needles and blood transfusion. un =Prevention * Vaccination - hepatitis A & B. * Always wash your hands thoroughly after using the restroom and when you come in contact with an infected person's blood, stools, or other bodily fluid. * Avoid unclean food and water. (can be infected by eating food or drinking water that has the hepatitis A virus in it). * avoid contact with other people's blood and body fluids. Don't share toothbrushes, razors and nail clippers. 7Vaccination Schedule by the Ministry of Health Malaysia un -